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目的：为进一步探讨运动性月经失调（ＡＭＩ）的机制提供理论依据。方法：在建立递增负荷训练的运动性闭经动物模型的基础上，对大鼠下丘脑弓状核神经元和垂体促性腺细胞超微结构进行观察。结果：电镜下，７周训练组大鼠下丘脑弓状核神经元轴突髓鞘分离、树突肿胀，核周质线粒体空泡变。垂体促性腺激素（Ｇｎ）细胞、生长激素（ＧＨ）细胞、促肾上腺皮质激素（ＡＣＴＨ）细胞的粗面内质网扩张，线粒体嵴断裂和肿胀。尤其是促性腺细胞粗面内质网极度扩张，出现类似性腺阉割细胞（Ⅳ型）和脱颗粒细胞（Ⅴ型）。休息１周后未见恢复。结论：运动性动情周期抑制发生在下丘脑水平，短期休息调整不能恢复。下丘脑－垂体轴细胞超微结构的改变与运动强度和运动时间密切相关。
Objective: To provide a theoretical basis for further discussion of the mechanism of exercise-induced menstrual disorders (AMI). Methods: The ultrastructural changes of hypothalamic arcuate nucleus neurons and pituitary gonadotrophs were observed on the basis of establishing a model of exercise-induced amenorrhea in rats. Results: Under electron microscope, the axons of arcuate nucleus of arcuate nucleus of hypothalamus in 7-week training group were separated, the dendrites were swollen and the mitochondrial vacuoles were changed. Pituitary gonadotropin (Gn) cells, growth hormone (GH) cells, rough endoplasmic reticulum expansion of adrenocorticotropic hormone (ACTH) cells, mitochondrial crista fractures and swelling. In particular, gonadal rough endoplasmic reticulum is extremely expanded, similar to glandular castrate cells (type Ⅳ) and degranulation cells (type Ⅴ). No recovery after 1 week of rest. Conclusion: The inhibition of exercise-induced estrous cycle occurs at hypothalamus level, and short-term rest adjustment can not be restored. Hypothalamus - pituitary axis ultrastructure changes and exercise intensity and exercise time are closely related.